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Scientists discover key driver of human
aging: May lead to slowing or reversing aging process

Date:

April 30, 2015

Source:

Salk Institute for Biological Studies

Summary:

A study tying the aging process to the
deterioration of tightly packaged bundles of cellular DNA could lead to methods
of preventing and treating age-related diseases such as cancer, diabetes and
Alzheimer's disease, experts say.

..........................

A study tying the aging process to the deterioration of tightly packaged
bundles of cellular DNA could lead to methods of preventing and treating
age-related diseases such as cancer, diabetes and Alzheimer's disease, as
detailed April 30, 2015, in Science.

In the study, scientists at the Salk Institute and the Chinese Academy of
Science found that the genetic mutations underlying Werner syndrome, a disorder
that leads to premature aging and death, resulted in the deterioration of
bundles of DNA known as heterochromatin.

The discovery, made possible through a combination of cutting-edge stem
cell and gene-editing technologies, could lead to ways of countering
age-related physiological declines by preventing or reversing damage to
heterochromatin.

"Our findings show that the gene mutation that causes Werner syndrome
results in the disorganization of heterochromatin, and that this disruption of
normal DNA packaging is a key driver of aging," says Juan Carlos Izpisua
Belmonte, a senior author on the paper. "This has implications beyond
Werner syndrome, as it identifies a central mechanism of aging--heterochromatin
disorganization--which has been shown to be reversible."

Werner syndrome is a genetic disorder that causes people to age more
rapidly than normal. It affects around one in every 200,000 people in the
United States. People with the disorder suffer age-related diseases early in
life, including cataracts, type 2 diabetes, hardening of the arteries,
osteoporosis and cancer, and most die in their late 40s or early 50s.

The disease is caused by a mutation to the Werner syndrome RecQ helicase-like
gene, known as the WRN gene for short, which generates the WRN protein.
Previous studies showed that the normal form of the protein is an enzyme that
maintains the structure and integrity of a person's DNA. When the protein is
mutated in Werner syndrome it disrupts the replication and repair of DNA and
the expression of genes, which was thought to cause premature aging. However,
it was unclear exactly how the mutated WRN protein disrupted these critical
cellular processes.

In their study, the Salk scientists sought to determine precisely how the
mutated WRN protein causes so much cellular mayhem. To do this, they created a
cellular model of Werner syndrome by using a cutting-edge gene-editing
technology to delete WRN gene in human stem cells. This stem cell model of the
disease gave the scientists the unprecedented ability to study rapidly aging
cells in the laboratory. The resulting cells mimicked the genetic mutation seen
in actual Werner syndrome patients, so the cells began to age more rapidly than
normal. On closer examination, the scientists found that the deletion of the
WRN gene also led to disruptions to the structure of heterochromatin, the
tightly packed DNA found in a cell's nucleus.

This bundling of DNA acts as a switchboard for controlling genes' activity
and directs a cell's complex molecular machinery. On the outside of the
heterochromatin bundles are chemical markers, known as epigenetic tags, which
control the structure of the heterochromatin. For instance, alterations to
these chemical switches can change the architecture of the heterochromatin,
causing genes to be expressed or silenced.

The Salk researchers discovered that deletion of the WRN gene leads to
heterochromatin disorganization, pointing to an important role for the WRN
protein in maintaining heterochromatin. And, indeed, in further experiments,
they showed that the protein interacts directly with molecular structures known
to stabilize heterochromatin--revealing a kind of smoking gun that, for the
first time, directly links mutated WRN protein to heterochromatin
destabilization.

"Our study connects the dots between Werner syndrome and
heterochromatin disorganization, outlining a molecular mechanism by which a
genetic mutation leads to a general disruption of cellular processes by
disrupting epigenetic regulation," says Izpisua Belmonte. "More
broadly, it suggests that accumulated alterations in the structure of
heterochromatin may be a major underlying cause of cellular aging. This begs
the question of whether we can reverse these alterations--like remodeling an
old house or car--to prevent, or even reverse, age-related declines and
diseases."

Izpisua Belmonte added that more extensive studies will be needed to fully
understand the role of heterochromatin disorganization in aging, including how
it interacts with other cellular processes implicated in aging, such as
shortening of the end of chromosomes, known as telomeres. In addition, the
Izpisua Belmonte team is developing epigenetic editing technologies to reverse
epigenetic alterations with a role in human aging and disease.







Story Source:

The above story is based on materials provided
by Salk Institute for Biological Studies. Note:
Materials may be edited for content and length.







Journal Reference:

1.   
Weiqi Zhang, Jingyi Li, Keiichiro Suzuki, Jing Qu, Ping Wang, Junzhi Zhou,
Xiaomeng Liu, Ruotong Ren, Xiuling Xu, Alejandro Ocampo, Tingting Yuan, Jiping
Yang, Ying Li, Liang Shi, Dee Guan, Huize Pan, Shunlei Duan, Zhichao Ding, Mo
Li, Fei Yi, Ruijun Bai, Yayu Wang, Chang Chen, Fuquan Yang, Xiaoyu Li, Zimei
Wang, Emi Aizawa, April Goebl, Rupa Devi Soligalla, Pradeep Reddy, Concepcion
Rodriguez Esteban, Fuchou Tang, Guang-Hui Liu, and Juan Carlos Izpisua
Belmonte. A Werner syndrome stem cell model unveils heterochromatin
alterations as a driver of human aging. Science, 30 April 2015
DOI:10.1126/science.aaa1356
sumber



http://www.sciencedaily.com/releases/2015/04/150430141803.htm

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